ライフサイエンスコーパス: gonococci

1 he challenges of antimicrobial resistance in gonococci.

2 le else is known about how AmiC functions in gonococci.

3 that become infected during transmission of gonococci.

4 morphonuclear leukocytes (PMN) with ingested gonococci.

5 predominantly inside the PMN in response to gonococci.

6 ting a bifunctional nature of this enzyme in gonococci.

7 ecular assay for detecting QRDR mutations in gonococci.

8 he survival disadvantage of MtrCDE-deficient gonococci.

9 of the farAB operon is modulated by MtrR in gonococci.

10 pumps to prevent their excess expression in gonococci.

11 than were wild-type or FarAB-MtrE-deficient gonococci.

12 % killing of otherwise fully serum-resistant gonococci.

13 ic, secretory, and recombination pathways of gonococci.

14 ruitment and co-localization of clathrin and gonococci.

15 le cloning step prior to transformation into gonococci.

16 irmed that all three ORFs are transcribed in gonococci.

17 er enhanced survival to hydrogen peroxide on gonococci.

18 pplied to native RNA isolated from wild-type gonococci.

19 roduct is an essential competence factor for gonococci.

20 fter infection with piliated and nonpiliated gonococci.

21 ruffles appear to be induced in response to gonococci.

22 d ASGP-R ligand decreased in the presence of gonococci.

23 begin to assess the sequence diversity among gonococci.

24 ss benefit to wild-type and mtrR(-79) mutant gonococci.

25 tests with probes to identify chlamydiae or gonococci.

26 and is at least as sensitive as culture for gonococci.

27 arkedly elongated during exposure to P+ Opa+ gonococci.

28 no acids important for binding to sialylated gonococci.

29 st complete conversion to iC3b on sialylated gonococci.

30 inidase-mediated cleavage of sialic acid off gonococci.

31 cipally responsible for its activity against gonococci.

32 aracterize the Tbp2 sequence diversity among gonococci.

33 , CHO cells are not capable of internalizing gonococci.

34 may contribute to cell tropism displayed by gonococci.

35 ufH contains the binding site for sialylated gonococci.

36 11 Opa variants and also bound Opa-negative gonococci.

37 5 volunteers became infected with sialylated gonococci.

38 tope-positive (but not 2C7 epitope-negative) gonococci.

39 l methods for the identification of possible gonococci.

40 which the lgt locus varies among strains of gonococci.

41 T4SS apparatus and intracellular survival of gonococci.

42 ey functional arm of NET-mediated killing of gonococci.

43 bound to CHO-CR3 and to unsialylated PorB.1A gonococci.

44 nuclear leukocytes (PMNs) with intracellular gonococci.

45 o increased in End/E6E7 cells incubated with gonococci.

46 ot fH from other primates, bound directly to gonococci.

47 of isogenic MtrR-positive and MtrR-negative gonococci.

48 nuclear leukocytes (PMNs) with intracellular gonococci.

49 e for release of peptidoglycan monomers from gonococci.

50 hat reported previously for sialylated Por1B gonococci.

51 recovered compared to the catalase-deficient gonococci.

52 enhanced serum sensitivity of Por1B-bearing gonococci.

53 the development of antibiotic resistance in gonococci.

54 However, the mechanisms by which gonococci acquire iron within this intracellular niche a

55 In the absence of FCS, OpaA+ gonococci adhered to but were not internalized by CHO ce

56 Piliated but not nonpiliated gonococci adhered to cells and produced up to an 80% red

57 Viable gonococci and chlamydiae were recovered for an average o

58 results indicate adherence between fH-coated gonococci and CR3 and may provide a means for gonococci

59 less of the proinflammatory PG monomers than gonococci and degrade PG to smaller fragments.

60 cell PK co-localizes with intracellular Opa+ gonococci and E. coli expressing Opa proteins.

61 Binding assays with gonococci and epithelial proteoglycan receptors revealed

62 site resulted in an increased resistance of gonococci and meningococci to the same compounds, as wel

63 The mutated genes have been transformed into gonococci and recombined into the chromosome.

64 ied this alternative FA resistance system in gonococci and report that it bears significant similarit

65 acid 1203 (N1203R) also bound to sialylated gonococci and restored killing.

66 present in FCS was binding to the surface of gonococci and subsequently stimulating entry.

67 ts involvement in FA resistance expressed by gonococci and to distinguish it from the emrAB- or vceAB

68 synthesis, fabA, fabM and fabB, was toxic in gonococci and unable to complement a NGO1024 mutation, s

69 s limited to cultures infected with piliated gonococci and was more vigorous in the endocervical epit

70 microscopy revealed lamellipodia surrounding gonococci, and confocal laser scanning microscopy analys

71 in situ contribute to the surface charge of gonococci, and they suggest that the bacterium's interac

72 rement for a genus-specific uptake sequence, gonococci appear capable of excluding DNA on the basis o

73 Expression of this phenotype by gonococci appears to rely on the expression of type IV p

74 quires enhanced transcription of mtrCDE when gonococci are grown in the presence of a sublethal conce

75 that the expression of mtrF is enhanced when gonococci are grown under inducing conditions.

76 sion assays, we demonstrated that PLD mutant gonococci are impaired in their ability to adhere to and

77 The data show that Opa-expressing gonococci are more efficient recipients of DNA for trans

78 gnostic nucleic acid amplification tests for gonococci are now in frequent use, molecular detection o

79 s membrane associated and surface exposed in gonococci, as shown by immunoblot analysis of soluble an

80 ance in determining the survival capacity of gonococci at mucosal surfaces that contain detergent-lik

81 nal lactobacilli have the ability to inhibit gonococci at two key steps of an infection, which might

82 of 6 volunteers inoculated with unsialylated gonococci became infected; however, only 1 of 5 voluntee

83 PorB.1B- and (unsialylated) PorB.1A-bearing gonococci bind fH through SCR 18 to 20; PorB.1A can also

84 Gonococci bind fH via their porin (Por) molecules (PorB.

85 Sialylated SS gonococci bound 4-fold less total C3 antigen than did SR

86 Nonsialylated SS gonococci bound 5-fold more C3b than did stably serum-re

87 Gonococci bound and were killed by wild-type HufH18-20/F

88 Por1B gonococci bound chimpanzee C4bp and resisted killing by

89 C3b bound later on stably SR gonococci but again was processed swiftly to iC3b.

90 ke protein-1 (contains fH SCRs 1-7) bound to gonococci but minimally to CHO-CR3.

91 pilin variants were longer than in parental gonococci but utilized the same donor pilS loci.

92 FCS) which is capable of mediating uptake of gonococci by CHO cells.

93 factor which mediates the internalization of gonococci by CHO cells.

94 articular, properdin in assisting killing of gonococci by specific Abs is the subject of this study.

95 Transforming DNA is donated by neighbouring gonococci by two different mechanisms: autolysis or type

96 The demonstration that gonococci can infect the lower genital tracts of estradi

97 l of mtrCDE gene expression, we propose that gonococci can modulate their resistance to HAs through b

98 tlA does not lyse gonococci expressing it or gonococci cocultured with an AtlA-expressing strain.

99 ed with native TbpA in the context of intact gonococci, consistent with surface exposure of the pepti

100 lly, but not aerobically, demonstrating that gonococci contain two distinct pathways for the producti

101 Internalized microcolonies, with P+ Opa+ gonococci, contained dividing cocci and appeared to be s

102 Pulse-chase experiments in gonococci demonstrated that LtgA produces a larger amoun

103 portant for the subsequent invasion step, as gonococci depleted for rpoH invade cells two- to threefo

104 wn to be important for the invasion step, as gonococci depleted for rpoH were reduced in their abilit

105 ant on mucosa and in purulent exudates, many gonococci do not express an Lf receptor.

106 ere we show that cyclical recovery of Opa(+) gonococci does not occur in ovariectomized mice; therefo

107 eparation and the release of PG fragments by gonococci during growth.

108 hat urethral epithelial cells are invaded by gonococci during the course of infection in males.

109 All gonococci encode a hemoglobin (Hgb) receptor, but it is

110 s study demonstrates that the lpxLII gene in gonococci encodes for a late-functioning lauroyl acyl tr

111 As gonococci encounter conditions of low iron during infect

112 esized to be an important mechanism by which gonococci evade host innate defenses.

113 This model proposes that gonococci express a surface feature that mimics human ch

114 Under most conditions encountered in vivo, gonococci express one or more opacity (Opa) proteins on

115 eferentially recognized the surface of whole gonococci expressing a homologous PorB, whereas serum fr

116 Gonococci expressing four gonococcal pilin variants with

117 red primary endometrial cells, together with gonococci expressing green fluorescent protein, has the

118 rs, 10 of 15 subjects became reinfected with gonococci expressing identical Por proteins.

119 f lysis demonstrated that AtlA does not lyse gonococci expressing it or gonococci cocultured with an

120 illed more rapidly than sialylated wild-type gonococci following intraperitoneal injection into norma

121 l, gonococci within vacuoles, and occasional gonococci free in the cytoplasm.

122 A significant increase of viable gonococci from 1 to 6 h was also observed, suggesting in

123 lactobacilli were able to displace adherent gonococci from epithelial cells, suggesting that these o

124 or the more rapid clearance of mtr-deficient gonococci from intact mice.

125 Among 72 pairs of gonococci from recent sexual contacts, the genotypes of

126 Strain F62 of Neisseria gonorrhoeae gonococci (GC) is sensitive to normal human serum unless

127 pa- and Opc- strains and also by nonpiliated gonococci (GC) that produce the invasion-associated OpaA

128 araldehyde-fixed eucaryotic cells to convert gonococci (GC) to this invasive phenotype (Inv+) is limi

129 + phenotypes when a mixture of Opa+ and Opa- gonococci (GC) was exposed to submaximal doses of NHS.

130 studies indicate that Neisseria gonorrhoeae (gonococci (GC)) has the capacity to enhance HIV type 1 (

131 (Stase) in Neisseria gonorrhoeae organisms (gonococci [GC]) transfers sialic acid (N-acetylneuramini

132 Neisseria gonorrhoeae cells (gonococci [GC]), the etiological agents for gonorrhea, c

133 n vivo, and staphylococci, streptococci, and gonococci have evolved mechanisms to utilize this glycop

134 sponse to and internalization of the P+ Opa+ gonococci; higher doses caused internalization without m

135 Further, gonococci highly resistant to ciprofloxacin were isolate

136 Growth of gonococci in a polysaccharide-free environment resulted

137 e and deglycosylated CD66e are recognized by gonococci in an Opa-specific manner.

138 idate Ab, attenuates vaginal colonization by gonococci in BALB/c mice.

139 bacilli in the female genital tract, inhibit gonococci in both acidic and neutral pH conditions.

140 These biofilms showed gonococci in networks of bacterial membrane within the b

141 t sigma(E), is important for the response of gonococci in the initial steps of an infection.

142 DNA is active in the transformation of other gonococci in the population and may act to transfer anti

143 The DNA is effective in transforming gonococci in the population, and this mechanism of DNA d

144 n-binding lipoprotein (TbpB) was detected on gonococci in vaginal smears, suggesting that although go

145 commensal lactobacilli may enhance growth of gonococci in vivo by promoting the solubilization of iro

146 ing of phenotypic and genotypic variation of gonococci in vivo.

147 2C7-mediated enhancement of C3 deposition on gonococci in vivo.

148 itric oxide likely is not protective against gonococci, in vivo; rather, nitric oxide may be required

149 tors associated with ciprofloxacin-resistant gonococci included: marital status, living alone, durati

150 hat infection of UECs with gentamicin-killed gonococci increased the expression of the antiapoptotic

151 C4bp alpha-chain monomers did not bind gonococci, indicating that the polymeric form of C4bp wa

152 a-OS, significantly impaired invasion of the gonococci into all three cell lines.

153 of LOS is required for efficient invasion of gonococci into host mucosa.

154 inhibitor prevented macropinocytic entry of gonococci into HUEC.

155 hat the association between lactobacilli and gonococci is complex and may be subject to factors that

156 A major peptidoglycan fragment released by gonococci is identical to the tracheal cytotoxin of Bord

157 Expression of the mtrCDE operon in gonococci is negatively regulated by the MtrR protein.

158 pecificity of factor H binding to sialylated gonococci is restricted to the LNT LOS species.

159 adherence and invasion) observed for mutant gonococci is, in part, attributed to the inability of th

160 Adherent gonococci lacking the pilus retraction protein PilT did

161 Gonococci make different LOS molecules, depending on whe

162 plexes as iron sources, indicating that some gonococci may express only the HmbR-independent hemoglob

163 ilus-negative (P-) Opa-, P- Opa+, or P+ Opa- gonococci, microvilli did not elongate, and the colonies

164 ore C3b than did stably serum-resistant (SR) gonococci; most was processed to iC3b, yet significant C

165 These results show that gonococci must express both pili and Opa to be engulfed

166 Gonococci often infect mucosal surfaces bathed in antiba

167 tentiate membrane ruffling and clustering of gonococci on the cervical cell surface.

168 ectin bound to the surface of OpaA-producing gonococci only and that the vitronectin-mediated uptake

169 and inoculated intravaginally with wild-type gonococci or a catalase (kat) deletion mutant.

170 arC86 alleles were introduced into wild-type gonococci or an isogenic mutant that is resistant to mac

171 epithelial cell membranes, and intracellular gonococci present in vacuoles.

172 osaccharide and converts to serum resistance gonococci previously sensitive to nonimmune serum killin

173 Gonococci producing a distinct opacity protein (OpaA in

174 serum, indicating that in biological fluids gonococci producing the heparin-binding Opa adhesin may

175 ibronectin was shown to bind specifically to gonococci producing the OpaA adhesin.

176 n the duration of infection or the number of gonococci recovered from untreated mice and mice coloniz

177 in vaginal smears, suggesting that although gonococci replicate within the genital tracts of mice, t

178 The mechanism(s) by which certain strains of gonococci resist normal human serum is not fully underst

179 with direct HufH binding, unsialylated Por1A gonococci resisted killing only by human complement, but

180 f mice infected with wild-type or kat mutant gonococci, respectively, and PMNs associated with numero

181 tion of the deletion mutation into wild-type gonococci resulted in lack of acetylation, and the pheno

182 Gonococci secrete chromosomal DNA into the extracellular

183 Rs (6, 7, and 18-20) bound to CHO-CR3 and to gonococci separately, but did not enhance bacteria-CR3 i

184 Gonococci shed by infected volunteers showed a transitio

185 , it became apparent that certain strains of gonococci showed differential incorporation of non-homol

186 Pil+ gonococci showed high levels of adherence and invasion,

187 Upon full depletion of oxygen, gonococci simultaneously switched into the low-speed mod

188 Reciprocal experiments (Opa- Cm(r) gonococci spiked with Opa+ Cm(s) bacteria) were consiste

189 The lipooligosaccharide (LOS) expressed by gonococci spontaneously varies its structure at high fre

190 non-opaque (P+Opa-, transparent) colony type gonococci, strain MS11mkC.

191 repeat (SCR1) bound to both Por1A and Por1B gonococci, suggesting that SCR1 contained Por binding si

192 were first detected 8 h after infection with gonococci, suggesting that the earlier IL-8 and IL-6 res

193 dative and non-oxidative killing mechanisms, gonococci survive this interaction, suggesting that the

194 /pilS recombination is shown to proceed with gonococci that carry inverted pilE loci.

195 Gonococci that possess one or more of a group of heat-mo

196 Direct-binding specificity of HufH only to gonococci that prevents serum killing is restricted to h

197 o bacterial cell surface charge, strain MS11 gonococci that were identical except for expressing a re

198 intravaginal inoculation with primarily Opa- gonococci, the majority of isolates recovered were Opa+

199 Unlike the situation with gonococci, the mtr system in meningococci is not subject

200 The process of DNA uptake in gonococci, therefore, is now known to require the expres

201 ovary (CHO) cells also support adherence of gonococci through interactions of OpaA with cell surface

202 is needed because of emerging resistance of gonococci to almost every class of antibiotic.

203 This mutation abrogated the ability of the gonococci to be transformed with chromosomal DNA.

204 uct enhanced binding of unsialylated PorB.1A gonococci to CHO-CR3.

205 omplex regulatory network in the response of gonococci to contact with host cells.

206 nal and spatial requirement for fH to bridge gonococci to CR3.

207 to be critically involved in the capacity of gonococci to develop chromosomally mediated resistance t

208 We previously showed that adherence of gonococci to epithelial cells results in changes of gene

209 expression is not necessary for adherence of gonococci to epithelial cells, it is important for the s

210 that NsrR plays a critical role in enabling gonococci to evade NO generated as a host defense mechan

211 act and that opa gene phase variation allows gonococci to evade or capitalize upon unidentified host

212 Resistance of gonococci to FAs and other antibacterial hydrophobic age

213 onococci and CR3 and may provide a means for gonococci to gain sanctuary into nonprofessional phagocy

214 L. jensenii inhibited the adherence of gonococci to glutaraldehyde-fixed epithelial cells like

215 eins, was found to result in an inability of gonococci to grow anaerobically.

216 Hb) receptor mutant (hpuAB mutant), allowing gonococci to grow on Hb as the sole source of iron.

217 he tonB homologue resulted in the failure of gonococci to grow with TF, LF or human haemoglobin (HB)

218 s act independently to mediate resistance of gonococci to host-derived, hydrophobic antimicrobial age

219 ial cells like it inhibited the adherence of gonococci to live epithelial cells, suggesting that the

220 hermore, it is shown that type IV pili allow gonococci to overcome the inhibitory effect of heparin,

221 be indicative of the inability of PLD mutant gonococci to recruit CR3 to the cervical cell surface.

222 on and that AtlA is not involved in lysis of gonococci to release DNA.

223 orrhoeae that is important in the ability of gonococci to resist certain hydrophobic antibiotics, det

224 fH to PorB and contributes to the ability of gonococci to resist complement-mediated killing.

225 ux systems may enable mucosal pathogens like gonococci to resist endogenous antimicrobial peptides th

226 nsight into the molecular mechanisms used by gonococci to scavenge Fe from TF and LF, we cloned a 3.5

227 The ability of gonococci to stimulate distinct proinflammatory host res

228 My data indicated that the ability of gonococci to survive and to replicate within pex cells w

229 irulence, and their sialylation would enable gonococci to survive within polymorphonuclear cells; how

230 However, the enhanced resistance of gonococci to TX-100 was dependent on the expression of a

231 The ability of Hgb+ gonococci to utilize hemoglobin as the iron source was a

232 mutation severely diminished the ability of gonococci to: (i) grow anaerobically; (ii) adapt to oxyg

233 Por1B loops 5 and 7 of serum-resistant gonococci together formed a negatively charged C4bp-bind

234 sion to host cells by either meningococci or gonococci triggers the rapid, localized formation of dra

235 e show that of the genes induced in adherent gonococci, two are part of the gonococcal RpoH regulon.

236 ng proteins; recent results demonstrate that gonococci unable to express transferrin- and lactoferrin

237 Gonococci undergo frequent and efficient natural transfo

238 mutS-deficient gonococci underwent an increased frequency of pilin anti

239 The differential effects of MMC and uvrD in gonococci unexpectedly reveal that MMC can function inde

240 e necessary for the up-regulation of rpoH in gonococci upon adherence to host cells.

241 ucted a genetic screen of transposon-mutated gonococci using a pilus-dependent colony morphology phen

242 this DNA is effective in transforming other gonococci via natural transformation.

243 ells by green fluorescent protein-expressing gonococci was characterized by colocalization of gonococ

244 Although the farAB system in gonococci was found to provide resistance to FAs indepen

245 Co-localization of ASGP-R with gonococci was observed.

246 rom mice inoculated with mutant or wild-type gonococci was reduced compared with that of the wild-typ

247 Serum resistance of gonococci was restored in these sera by human C4bp.

248 by the selection pattern shown by wild-type gonococci, we demonstrated that a constitutive Opa-expre

249 Some gonococci were cleared in the first 30 to 60 min after p

250 fH domains necessary for binding sialylated gonococci were determined by incubating organisms with r

251 The gonococci were effectively bound and engulfed by B cells

252 , the local and systemic immune responses to gonococci were extremely modest.

253 Consistent with membrane ruffling, gonococci were found residing within macropinosomes, and

254 However, Lst-deficient gonococci were killed more rapidly than sialylated wild-

255 iectomized mice showed that MtrCDE-deficient gonococci were more rapidly cleared from mice that were

256 As reported for human PMNs, sialylated gonococci were more resistant to killing by murine PMNs,

257 MtrCDE-deficient gonococci were more sensitive to nonphysiological concen

258 Finally, as previously reported, Opa(+) gonococci were more sensitive to serine proteases.

259 Interestingly, significantly more gonococci were recovered from coinfected mice compared t

260 cal and mucosal isolates of meningococci and gonococci were shown to bind to the CD66 N-domain, demon

261 Electron microscopy showed that agar-grown gonococci were surrounded by a coat of alcian blue-posit

262 To facilitate these studies, gonococci were transformed with a hybrid shuttle vector

263 When gonococci were transformed with chromosomal donor DNA co

264 e of substantially higher antibody levels to gonococci where there is infection at a site known to co

265 und 4-fold less total C3 antigen than did SR gonococci, which was promptly converted to iC3b.

266 ntal transmission of chromosomal DNA between gonococci will favour the spread of intact alleles, as o

267 The recognition that gonococci with certain phenotypes can recruit surface po

268 ia were studied to investigate the spread of gonococci with decreased fluoroquinolone susceptibility.

269 Strains of gonococci with decreased susceptibility to ciprofloxacin

270 clinic in Cleveland, Ohio, the prevalence of gonococci with decreased susceptibility to ciprofloxacin

271 cocci was characterized by colocalization of gonococci with F actin, which were initially detected 30

272 Pilus-mediated interactions of gonococci with human epithelial cells results in a patho

273 ortance of Arg-1203 by incubating sialylated gonococci with normal human serum, in the presence of wi

274 vious work to investigate the interaction of gonococci with primary human cervical epithelial (pex) c

275 man challenge experiment, the infectivity of gonococci with sialylated lipooligosaccharide (LOS) was

276 These results show that gonococci with sialylated LOS are less infective than go

277 with sialylated LOS are less infective than gonococci with unsialylated LOS.

278 e (LOS) was compared with the infectivity of gonococci with unsialylated LOS.

279 ween the gonococcus and the epithelial cell, gonococci within vacuoles, and occasional gonococci free